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The study confirms that the N2 and P3 NoGo effects are not solely due to movement-related potentials, and posits the NoGo P3 as a marker of motor inhibition.

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The role of afferent inflow and efferent outflow (or command) signals in judgements of limb position has been debated for over a century. One way to assess this is to check for changes during complete paralysis, with the current view being that perceived movements or position changes do not usually accompany attempts to contract paralysed muscles. To re-examine this, we asked six naïve subjects to carry out a simple position-matching task at the wrist. In the absence of vision, subjects accurately perceived the position to which their right wrist had been moved by the experimenter by matching it with their left hand. There was no significant change in perception when position was matched during sustained flexion or extension efforts. Then we paralysed and anaesthetized the right arm with ischaemia in order to produce a 'phantom' hand. The perceived position of the wrist changed by more than 20 deg when subjects attempted to flex or extend their hand when it was paralysed and anaesthetized. Further studies showed that this illusion was not dependent on the way in which the paralysis was produced and that the size of the position illusion increased when the level of effort during paralysis increased. These results establish for the first time a definitive role for 'outflow' signals in position sense.

The role of group III and IV muscle afferents in controlling the output from human muscles is poorly understood. We investigated the effects of these afferents from homonymous or antagonist muscles on motoneuron pools innervating extensor and flexor muscles of the elbow. In study 1, subjects (n ϭ 8) performed brief maximal voluntary contractions (MVCs) of elbow extensors before and after a 2 min MVC of the extensors. During MVCs, electromyographic responses from triceps were evoked by stimulation of the corticospinal tracts [cervicomedullary motor evoked potentials (CMEPs)]. The same subjects repeated the protocol, but input from fatigue-sensitive afferents was prolonged after the fatiguing contraction by maintained muscle ischemia. In study 2, CMEPs were evoked in triceps during brief extensor MVCs before and after a 2 min sustained flexor MVC (n ϭ 7) or in biceps during brief flexor MVCs before and after a sustained extensor MVC (n ϭ 7). Again, ischemia was maintained after the sustained contractions. During sustained MVCs of the extensors, CMEPs in triceps decreased by ϳ35%. Without muscle ischemia, CMEPs recovered within 15 s, but with maintained ischemia, they remained depressed (by ϳ28%; p Ͻ 0.001). CMEPs in triceps were also depressed (by ϳ20%; p Ͻ 0.001) after fatiguing flexor contractions, whereas CMEPs in biceps were facilitated (by ϳ25%; p Ͻ 0.001) after fatiguing extensor contractions. During fatigue, inputs from group III and IV muscle afferents from homonymous or antagonist muscles depress extensor motoneurons but facilitate flexor motoneurons. The more pronounced inhibitory influence of these afferents on extensors suggests that these muscles may require greater cortical drive to generate force during fatigue.

The findings suggest the need for a major review of current interpretations of the N2 and P3 in inhibitory tasks.

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